Adenovirus in Falcons: Diagnostic Assays and Outbreak Prevention
American Association of Zoo Veterinarians Conference 2004
Mark Schrenzel1, DVM, PhD, DACVP; Lindsay Oaks2, DVM, PhD, DACVM; Dave Rotstein3, DVM, MPVM, DACVP; Gabriel Maalouf1, BS; Eric Snook1, DVM; Cal Sandfort4; Bruce Rideout1, DVM, PhD, DACVP
1Department of Pathology, Center for Reproduction of Endangered Species, Zoological Society of San Diego, San Diego, CA, USA; 2Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA, USA; 3Department of Pathobiology, School of Veterinary Medicine, University of Tennessee, Knoxville, TN, USA; 4The Peregrine Fund, Boise, ID, USA

Abstract

Adenoviruses are morphologically, genetically and biologically diverse agents that have been identified by ultrastructural or molecular methods in fish, birds, reptiles, mammals, and amphibia.1,2,5 Most natural infections are subclinical and require co-infection with viral or bacterial pathogens, toxin exposure, or immune compromise to the host for significant disease to occur.6,7 Occasionally, however, emergent viral strains, cross-species transmission, or high-dose infection of young, naive animals result in severe disease without the presence of cofactors.4

In birds, detailed molecular and cellular analyses have been done on the adenovirus type species of group I (fowl adenovirus 1 of chickens), group II (hemorrhagic enteritis virus of turkeys), and group III (egg drop syndrome virus of chickens) viruses of poultry.6 In the genus Falco, adenovirus has been described in a merlin (Falco columbarius), seven American kestrels (Falco sparverius) and 13 Mauritius kestrels (Falco punctatus).3,8,9 These studies brought attention to the danger of adenoviruses in captive falcons but were limited to morphologic descriptions of viral particles and lesions in affected birds. The source, genotype, involvement of co-pathogens, and interspecies communicability of falconid adenoviruses have not been reported.

In 1996 at a captive breeding facility in Idaho, anorexia, dehydration, and diarrhea or sudden death occurred in Northern aplomado falcons (Falco femoralis septentrionalis) from 9 to 35 days of age and peregrine falcons (Falco peregrinus) from 14 to 25 days of age. Sixty-two northern aplomado and six peregrine falcons died. Epidemiologic analyses indicated a point source epizootic, horizontal transmission and increased relative risk associated with cross-species brooding of eggs. Affected birds had inclusion body hepatitis, splenomegaly and enteritis. The etiology in all mortalities was determined by molecular analyses to be a new species of adenovirus distantly related to the group I avian viruses, serotypes 1 and 4, genus Aviadenovirus. In situ hybridization and polymerase chain reaction (PCR) demonstrated that the virus was epitheliotropic and lymphotropic and that infection was systemic in the majority of animals.

Adeno-associated virus was also detected by PCR in most affected falcons, but no other infectious agents or predisposing factors were found in any birds. Subsequent to the 1996 epizootic, similar disease caused by the same adenovirus was found in three other falcon species: two orange-breasted falcons (Falco deiroleucus), two Teita falcons (Falco fasciinucha) and a merlin (Falco columbarius), a peregrine falcon subspecies (Falco peregrinus nesiotes), and two gyrfalcon X peregrine falcon hybrids (Falco rusticolus/peregrinus) from Wyoming, Minnesota, Oklahoma and California, respectively. The adenovirus appeared to be the primary cause of disease and death in all birds. A specific and sensitive PCR for detection of this adenovirus in feces or tissues is now available at the on-site Molecular Diagnostics Laboratory (Zoological Society of San Diego, San Diego, CA) and is a valuable method for screening animals and preventing future outbreaks.

Literature Cited

1.  Benko M. and B. Harrach. 2003. Molecular evolution of adenoviruses. Curr. Topics Microbiol. Immunol. 272: 3–35.

2.  Davison A.J., K.M. Wright, and B. Harrach. 2000. DNA sequence of frog adenovirus. J. Gen. Virol. 81: 2431–2439.

3.  Forbes, N.A., G.N. Simpson, R.J. Higgins, and R.E. Gough. 1997. Adenovirus infection in Mauritius kestrels (Falco punctatus). J. Avian Med.Surg. 11: 31–33.

4.  Guy J.S., J.L. Schaeffer, and H.J. Barnes. 1988. Inclusion-body hepatitis in day-old turkeys. Avian Dis. 32: 587–590.

5.  Hess M. 2000. Detection and differentiation of avian adenoviruses: a review. Avian Pathol. 29: 195–206.

6.  McFerran J.B. 2003. Adenovirus infections. In: Saif YM (ed). Diseases of Poultry, 11th ed. Iowa State University Press, Ames, IA. Pp 213–251.

7.  Nemerow G.R., and P.L. Stewart. 1999. Role of alpha integrins in adenovirus cell entry and gene delivery. Microbiol. Molec. Biol. Rev. 63: 725–734.

8.  Schelling S.H., D.S. Garlick, and J. Alroy. 1989. Adenoviral hepatitis in a merlin (Falco columbarius). Vet. Pathol. 26: 529–530.

9.  Sileo, L., J.C. Franson, D.L. Graham, C.H. Domermuth, B.A. Rattner, and O.H. Pattee. 1983. Hemorrhagic enteritis in captive American kestrels (Falco sparverius). J. Wildl. Dis. 19: 244–247.

 

Speaker Information
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Mark Schrenzel, DVM, PhD, DACVP
Department of Pathology
Center for Reproduction of Endangered Species
Zoological Society of San Diego
San Diego, CA, USA


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